The last intron, which is responsible for the limitation of transposase activity to the germline, has been deleted. P\TΔ2-3 therefore produces transposase in both the somatic and germ cells.
P\TΔ2-3 lacks a tissue-specific intron that normally limits transposase activity to the germline.
Precise deletion of the intron sequences at the ORF2 and ORF3 junction.
P{KP}2F represses the transposase activity of P{Δ2-3}99B in the germline; the rate of snw mutation in the male germline caused by P{Δ2-3}99B is reduced if P{KP}2F is present. H{hsp/KP} represses the transposase activity of P{Δ2-3}99B in the germline; the rate of snw mutation in the male germline caused by P{Δ2-3}99B is reduced if H{hsp/KP} is present. P{KP}13F does not repress the transposase activity of P{Δ2-3}99B in the germline; the rate of snw mutation in the male germline caused by P{Δ2-3}99B is not affected if P{KP}13F is present.
No repression of P-element mobility in somatic tissues.
Transposase activity is present in the germline and soma.
P\TΔ2-3 produces transposase, but is not mobile.
Assayed for transposase activity in the germline using the snw assay. Assayed for transposase activity in the soma using the snw and P{wA}038 assays.
Distribution of male recombination events, in the absence of P element targets, approximates that seen in studies of radiation-induced crossing-over. Where there is a single P element target, P{lArB}A53.1M3, crossovers increased 58-fold in the immediate region of the P element target.
99B insert consists of two copies of the original insert in head-to-head orientation with approximately 360bp missing from the junction of the 5' P-element ends (1-19 of one 5' end and 1-348 of the other). Stability of the insertion can be explained by the insert having two functional 3' ends (mobilisation of an insertion with symmetrical ends by transposase is less efficient) and the composite element is 20kb long again causing less efficient mobilisation. Resultant composite element has one functional P\T gene and two copies of ry+t7.2.